ArticlePloS one2016
ER Alpha Rapid Signaling Is Required for Estrogen Induced Proliferation and Migration of Vascular Endothelial Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Gut Dysbiosis, Sex, and Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysms.Current atherosclerosis reports · 2026Review
- Does the Menstrual Phase Matter in Vascular Endothelial Responses to Acute Exercise? A Narrative Review of the Literature.Sports (Basel, Switzerland) · 2025Review
- Sex-dependent Pathophysiology and Therapeutic Considerations in Right Heart Disease.The Canadian journal of cardiology · 2025Review
- Hormone Replacement Therapy and Cardiovascular Health in Postmenopausal Women.International journal of molecular sciences · 2025Review
- Estrogen Inhibits the Phenotypic Switching of Vascular Smooth Muscle Cells through ER-α/CREB in Aortic Dissection.ACS omega · 2025Article
- Sex bias in tumor immunity: insights from immune cells.Theranostics · 2025Review
- Endothelial oestrogen-myocardial cyclic guanosine monophosphate axis critically determines angiogenesis and cardiac performance during pressure overload.Cardiovascular research · 2024Article
- Nongenomic ERα-AMPK Signaling Regulates Sex-Dependent Bcrp Transport Activity at the Blood-Brain Barrier.Endocrinology · 2024Article
- Sex-specific differences in the clinical profile among psychiatric patients with pulmonary Embolism: a hospital-based retrospective study.BMC pulmonary medicine · 2024Article
- Endothelial ERα promotes glucose tolerance by enhancing endothelial insulin transport to skeletal muscle.Nature communications · 2023Article
- β-Estradiol 17-acetate enhances theNeural regeneration research · 2023Article
- The emerging role of estrogen's non-nuclear signaling in the cardiovascular disease.Frontiers in cardiovascular medicine · 2023Review
- Estrogen signaling as a bridge between the nucleus and mitochondria in cardiovascular diseases.Frontiers in cell and developmental biology · 2022Review
- Estrogen receptors, ERKFrontiers in physiology · 2022Article
- Endocrine disorders and fertility and pregnancy: An update.Frontiers in endocrinology · 2022Review
- Estrogens and the regulation of glucose metabolism.World journal of diabetes · 2021Review
- Estrogen activates endothelial exocytosis.Biochemical and biophysical research communications · 2021Article
- Signalling mechanisms in the cardiovascular protective effects of estrogen: With a focus on rapid/membrane signalling.Current research in physiology · 2021Review
- Sex Differences and Regulatory Actions of Estrogen in Cardiovascular System.Frontiers in physiology · 2021Review
- Sex differences in cancer mechanisms.Biology of sex differences · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Estrogen promotes the proliferation and migration of vascular endothelial cells (ECs), which likely underlies its ability to accelerate re-endothelialization and reduce adverse remodeling after vascular injury. In previous studies, we have shown that the protective effects of E2 (the active endogenous form of estrogen) in vascular injury require the estrogen receptor alpha (ERα). ERα transduces the effects of estrogen via a classical DNA binding, "genomic" signaling pathway and via a more recently-described "rapid" signaling pathway that is mediated by a subset of ERα localized to the cell membrane. However, which of these pathways mediates the effects of estrogen on endothelial cells is poorly understood. Here we identify a triple point mutant version of ERα (KRR ERα) that is specifically defective in rapid signaling, but is competent to regulate transcription through the "genomic" pathway. We find that in ECs expressing wild type ERα, E2 regulates many genes involved in cell migration and proliferation, promotes EC migration and proliferation, and also blocks the adhesion of monocytes to ECs. ECs expressing KRR mutant ERα, however, lack all of these responses. These observations establish KRR ERα as a novel tool that could greatly facilitate future studies into the vascular and non-vascular functions of ERα rapid signaling. Further, they support that rapid signaling through ERα is essential for many of the transcriptional and physiological responses of ECs to E2, and that ERα rapid signaling in ECs, in vivo, may be critical for the vasculoprotective and anti-inflammatory effects of estrogen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.